Effects of perioperative intravenous lidocaine and esketamine on the quality of recovery and emotional state of patients after thyroidectomy: A randomised, double-blind, controlled trial.

Background and Aims: Perioperative intravenous (IV) infusions of lidocaine and esketamine reduce postoperative pain, but there are few studies on the quality of recovery and patients' emotional states postoperatively. We aimed to explore the effects of perioperative IV lidocaine and esketamine on the quality of recovery and emotional state after thyroidectomy. Methods: In this randomised trial, 137 patients undergoing thyroidectomy were randomly assigned to three groups: a lidocaine group (Group L), an esketamine group (Group E) and a normal saline placebo group (Group C). The primary outcome was the Quality of Recovery 40 (QoR-40) on postoperative days (PODs) 1 and 2. The secondary outcomes included Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS) scores on days 1 and 2 after surgery, pain scores, opioid consumption and incidence of postoperative nausea and vomiting (PONV). Statistical analysis was performed using the one-way analysis of variance (ANOVA), the Kruskal-Wallis and Chi-square tests. Results: The global QoR-40 scores in groups L and E on POD 1 and POD 2 were significantly higher than in group C (P < 0.001). The SAS and SDS scores on POD 1 and POD 2 in groups L and E were significantly lower than in group C (P < 0.05). There were statistically significant differences in Numerical Rating Scale (NRS) scores among the three groups at 1 h, 2 h, 6 h and 12 h (P < 0.05). Conclusion: Perioperative IV lidocaine and esketamine improve the quality of postoperative recovery and the emotional state of patients undergoing thyroidectomy.

Effect of ultrasound-guided bilateral superficial cervical plexus block versus perioperative intravenous lidocaine infusion on postoperative quality of recovery in patients undergoing thyroidectomy: A randomised double-blind comparative trial.

Background and Aims: Recent studies have found that ultrasound-guided (USG) bilateral superficial cervical plexus block (BSCPB) and intravenous infusion of lidocaine (IVL) have the potential to improve the quality of postoperative recovery. This study aimed to investigate and compare their effects on postoperative quality of recovery in patients undergoing thyroidectomy. Methods: A total of 135 patients were randomised to Group N: BSCPB with 10 mL 0.75% ropivacaine on each side, Group L: intravenous lidocaine (1.5 mg/kg for 10 min, followed by 1.5 mg/kg/h) and Group C: intravenous saline combined with BSCPB saline. The primary objective was quality of recovery-40 (QoR-40). Other parameters compared were numeric rating pain scale (NRS) score, haemodynamic data, opioid dosage and incidence of adverse effects. Statistical analysis was performed using the one-way analysis of variance (ANOVA), the Kruskal-Wallis test and the Chi-square test. Results: Compared to Group C, both groups N and L had higher QoR-40 total scores as well as scores indicating physical comfort, emotional state and pain dimensions on postoperative day (POD) 1 and POD2 (P < 0.001). The QoR-40 total and pain dimension scores in Group N were higher on POD1 and POD2 (P < 0.05). The NRS scores and the change in haemodynamics were lower in Group N compared to groups L and C (P < 0.05). The results of other parameters were lower in groups N and L than in Group C (P < 0.05). Conclusion: USG BSCPB and IVL are comparable in improving the quality of postoperative recovery in patients undergoing thyroidectomy.

Organic metal matrix Mil-88a nano-enzyme for joint repair in the osteoarthritis mouse model.

Introduction: In this paper we tried to conduct a novel nanomaterial strategy to overcome osteoarthritis (OA) in a mouse model. Methods: In this regard, after synthesizing the Mil-88a nanozyme, as a certain Fe-MOF, its toxic effects were detected by CCK-8 method and live-dead staining. The OA model of mouse was constructed, and paraffin sections of joints were taken for histological evaluation. In addition, immunofluorescence and immunohistochemistry were used to identify the OA progression and OARSI was used to evaluate the OA grades. We observed that Mil-88a could be easily synthesized and has high biocompatibility. Results: We observed that Mil-88a could significantly promote the expression of OA anabolism-related genes such as Col2 and also significantly inhibit the expression of OA catabolism-related genes MMP13. Besides, we observed better OARSI score in animals treated with Mil-88a nano-enzyme loading on organic metal matrix. Discussion: Overall, Mil-88a nano-enzyme could be used as a novel strategy to treat OA.

Fraxetin suppresses reactive oxygen species-dependent autophagy by the PI3K/Akt pathway to inhibit isoflurane-induced neurotoxicity in hippocampal neuronal cells.

Isoflurane, a common volatile anesthetic, has been widely used to provide general anesthesia in operations. However, exposure to isoflurane may cause widespread neurotoxicity in the developing animal brain. Fraxetin, a natural coumarin derivative extracted from the bark of Fraxinus rhynchophylla, possesses versatile pharmacological properties including anti-oxidative, anti-inflammatory, and neuroprotective effects. However, the effect and action mechanism of fraxetin on neurotoxicity induced by isoflurane are unknown. Reactive oxygen species (ROS) generation, cell viability, lactate dehydrogenase (LDH) release, and apoptosis were estimated by 2',7'-dichlorofluorescin-diacetate (DCFH-DA) staining, MTT, LDH release, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) staining assays, respectively. The protein levels of light chain 3 (LC3)-I, LC3-II, p62, protein kinase B (Akt), and phosphorylated Akt (p-Akt) were detected by western blot analysis. Isoflurane induced ROS, LDH release, apoptosis, and autophagy, but inhibited the viability in HT22 cells, which were overturned by fraxetin or ROS scavenger N-acetyl-L-cysteine. Fraxetin suppressed isoflurane-induced PI3K/Akt inactivation in HT22 cells. PI3K/Akt inactivation by LY294002 resisted the effects of fraxetin on isoflurane-induced autophagy and autophagy-modulated neurotoxicity in HT22 cells. In conclusion, fraxetin suppressed ROS-dependent autophagy by activating the PI3K/Akt pathway to inhibit isoflurane-induced neurotoxicity in hippocampal neuronal cells.

Knockdown of Linc00052 alleviated spinal nerve ligation-triggered neuropathic pain through regulating miR-448 and JAK1.

The dysfunction of the nervous system contributes to neuropathic pain. Long noncoding RNAs are reported to participate in neuropathic pain. Recently, Linc00052 is implicated to be closely associated with multiple diseases. Nevertheless, the mechanisms of Linc00052 remain barely explored in neuropathic pain development. Currently, spinal nerve ligation (SNL) triggered neuropathic pain was employed in our investigation. Here, we assessed the function of Linc00052 in SNL rat models. Interestingly, we reported Linc00052 was significantly elevated in SNL rats. Loss of Linc00052 could reduce neuropathic pain progression via regulating the behaviors of neuropathic pain. Additionally, knockdown of Linc00052 repressed the processes of neuroinflammation. Interleukin (IL)-6 and tumor necrosis factor α level were inhibited while IL-10 was induced by the silence of Linc00052. Moreover, we predicted miR-448 can serve as a target of Linc00052. miR-448 exerts a crucial power in several diseases. Currently, we exhibited miR-448 was remarkably downregulated in SNL rats. RNA immunoprecipitation experiments validated the association between miR-448 and Linc00052. Inhibition of Linc00052 could reverse the roles of miR-448 on neuropathic pain development. Furthermore, Janus kinase 1 (JAK1) was displayed as the putative target of miR-448 in the present investigation. It was showed that JAK1 was induced in SNL rats. Loss of miR-448 could dramatically induce the expression of JAK1, which was rescued by knockdown of Linc00052. Taken these together, our study implied that Linc00052 functioned as a novel target of neuropathic pain via sponging miR-448 and regulating JAK1.

miR-194 relieve neuropathic pain and prevent neuroinflammation via targeting FOXA1.

The emerging role of microRNAs (miRNAs) have been deeply explored in multiple diseases including neuropathic pain. miR-194 was widely reported to be a tumor suppressor and was related to the inflammatory response. The critical role of neuroinflammation on neuropathic pain leads to a thinking about the relationship between miR-194 and neuropathic pain. However, the function of miR-194 in neuropathic pain remains unknown. This study was aimed to explore the relationship between miR-194 and neuropathic pain progression by chronic sciatic nerve injury (CCI). miR-194 abnormally downregulated in the CCI model rat and its overexpression significantly alleviates neuroinflammation in vivo. We predict Forkhead box protein A1 (FOXA1) as a direct target of miR-194, whose restoration can markedly reverse the effects of miR-194 on neuropathic pain. Overall, our study demonstrated a novel mechanism of neuropathic pain progression that miR-194 alleviates neuropathic pain via targeting FOXA1 and preventing neuroinflammation by downregulating inflammatory cytokines containing cyclooxygenase 2, interleukin 6 (IL-6), and IL-10 in vivo, which can be reversed by the overexpression of FOXA1.